mutant mice (Fig. 4b). Expression of the myelin-associated genes such as Plp1 (Fig. 4c, d) and Mbp (Supplementary Fig. 5c, d) were decreased in the lesion areas of mutant mice. Ultrastructural analyses on the lesions again revealed markedly lower percentage of remyelinated axons and thinner myelin sheaths in the mutants than that of the controls (Figs. 4e–g). To quantitively evaluate the newly differentiated OLs during myelin regeneration, BrdU was added to label all the proliferative OPCs after LPC injury (Fig. 4a). The total number of CC1+ cell was only slightly declined, but new born OLs (BrdU+ CC1+) was almost vanished in corpus callosum of Setdb1 mutant mice (Figs. 4h–j). Altogether, our data clear demonstrate that both myelination and remyelination are reliant on the repressive function of OLIG2-SETDB1 complex.
